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Reverse Takotsubo Cardiomyopathy After Treatment of Asymptomatic Bradycardia Prior to Anesthesia Induction in a Young
Samantha Henry1, Kelly Rothbart1, Amit Prasad1
1Heart and Vascular Critical Care Unit, Heart and Vascular Institute, Penn State Health, Hershey, PA, USA.
Abstract:
BACKGROUND Reverse takotsubo cardiomyopathy is a rare stress-induced variant of cardiomyopathy characterized by hypokinesis of the basal and midventricular segments of the left ventricle and apical hyperkinesis. CASE REPORT Takotsubo cardiomyopathy, or "broken heart syndrome," is a stress-induced cardiomyopathy defined by regional wall motion abnormalities of the left ventricle without evidence of coronary artery disease. Typically, these abnormalities affect the apex of the left ventricle, mimicking myocardial infarction and occasionally presenting with elevated troponin. A rare variant, reverse takotsubo cardiomyopathy, involves hypokinetic basal and midventricular segments of the left ventricle with apical hyperkinesis. We report the case of a 27-year-old woman who experienced cardiac arrest shortly after administration of glycopyrrolate for asymptomatic bradycardia prior to anesthesia induction for elective rhinoplasty. The glycopyrrolate induced tachycardia, ultimately resulting in cardiac arrest that required advanced cardiac life support and chest compressions. Return of spontaneous circulation was achieved, and the patient was transferred to the cardiac intensive care unit in cardiogenic shock. Echocardiography initially demonstrated an ejection fraction of 42%. Subsequent echocardiography showed a newly reduced ejection fraction of 25% and basal hypokinesis with apical hyperkinesis, consistent with reverse takotsubo cardiomyopathy. Although the patient was evaluated for cardiac transplantation, she fully recovered via supportive therapy, including inotropes and vasopressors, within approximately 1 week. CONCLUSIONS The temporal association between glycopyrrolate administration and symptom onset suggests that a drug-induced catecholamine surge triggered severe myocardial dysfunction, resulting in cardiogenic shock.
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